TY - JOUR
T1 - Neurocircuitry Models of Posttraumatic Stress Disorder and Extinction
T2 - Human Neuroimaging Research-Past, Present, and Future
AU - Rauch, Scott L.
AU - Shin, Lisa M.
AU - Phelps, Elizabeth A.
N1 - Funding Information:
SLR and LMS are supported in part by National Institute of Mental Health (NIMH) Grant R21MH72156; LMS is supported in part by a National Alliance for Research on Schizophrenia and Depression (NARSAD) Young Investigator Award; EAP is supported by NIMH Grants R21MH072279 and RO1MH62104.
Funding Information:
Aspects of this work were presented at Extinction: The Neural Mechanisms of Behavior Change, February 2-6, 2005, Ponce, Puerto Rico. The conference was sponsored by the National Institute of Mental Health, National Institute of Drug Abuse, Ponce School of Medicine, University of Puerto Rico COBRE Program, Pfizer Global Pharmaceutical, and the Municipality of Ponce.
PY - 2006/8/15
Y1 - 2006/8/15
N2 - The prevailing neurocircuitry models of anxiety disorders have been amygdalocentric in form. The bases for such models have progressed from theoretical considerations, extrapolated from research in animals, to in vivo human imaging data. For example, one current model of posttraumatic stress disorder (PTSD) has been highly influenced by knowledge from rodent fear conditioning research. Given the phenomenological parallels between fear conditioning and the pathogenesis of PTSD, we have proposed that PTSD is characterized by exaggerated amygdala responses (subserving exaggerated acquisition of fear associations and expression of fear responses) and deficient frontal cortical function (mediating deficits in extinction and the capacity to suppress attention/response to trauma-related stimuli), as well as deficient hippocampal function (mediating deficits in appreciation of safe contexts and explicit learning/memory). Neuroimaging studies have yielded convergent findings in support of this model. However, to date, neuroimaging investigations of PTSD have not principally employed conditioning and extinction paradigms per se. The recent development of such imaging probes now sets the stage for directly testing hypotheses regarding the neural substrates of fear conditioning and extinction abnormalities in PTSD.
AB - The prevailing neurocircuitry models of anxiety disorders have been amygdalocentric in form. The bases for such models have progressed from theoretical considerations, extrapolated from research in animals, to in vivo human imaging data. For example, one current model of posttraumatic stress disorder (PTSD) has been highly influenced by knowledge from rodent fear conditioning research. Given the phenomenological parallels between fear conditioning and the pathogenesis of PTSD, we have proposed that PTSD is characterized by exaggerated amygdala responses (subserving exaggerated acquisition of fear associations and expression of fear responses) and deficient frontal cortical function (mediating deficits in extinction and the capacity to suppress attention/response to trauma-related stimuli), as well as deficient hippocampal function (mediating deficits in appreciation of safe contexts and explicit learning/memory). Neuroimaging studies have yielded convergent findings in support of this model. However, to date, neuroimaging investigations of PTSD have not principally employed conditioning and extinction paradigms per se. The recent development of such imaging probes now sets the stage for directly testing hypotheses regarding the neural substrates of fear conditioning and extinction abnormalities in PTSD.
KW - Ventromedial prefrontal cortex
KW - amygdala
KW - anterior cingulate cortex
KW - anxiety disorders
KW - fear conditioning
KW - hippocampus
KW - magnetic resonance imaging
KW - orbitofrontal cortex
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U2 - 10.1016/j.biopsych.2006.06.004
DO - 10.1016/j.biopsych.2006.06.004
M3 - Review article
C2 - 16919525
AN - SCOPUS:33747051450
SN - 0006-3223
VL - 60
SP - 376
EP - 382
JO - Biological Psychiatry
JF - Biological Psychiatry
IS - 4
ER -